Laron syndrome pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | |||
Molecular genetic investigations have shown that this disorder is mainly associated with mutations in the gene for the GH receptor. These can result in defective hormone binding to the ectodomain or reduced efficiency of dimerization of the receptor after hormone occupancy. There are exceptionally low levels of [[insulin growth factor]] ([[IGF-1]]) and its principal [[carrier protein]], [[insulin-like growth factor binding protein 3]]. Laron syndrome is a [[autosomal recessive]] disorder. | |||
==References== | ==References== | ||
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[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
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Latest revision as of 19:56, 19 September 2012
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Laron syndrome Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Laron syndrome pathophysiology On the Web |
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American Roentgen Ray Society Images of Laron syndrome pathophysiology |
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Risk calculators and risk factors for Laron syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Molecular genetic investigations have shown that this disorder is mainly associated with mutations in the gene for the GH receptor. These can result in defective hormone binding to the ectodomain or reduced efficiency of dimerization of the receptor after hormone occupancy. There are exceptionally low levels of insulin growth factor (IGF-1) and its principal carrier protein, insulin-like growth factor binding protein 3. Laron syndrome is a autosomal recessive disorder.